ReviewOxidative medicine and cellular longevity2020
Antioxidants Targeting Mitochondrial Oxidative Stress: Promising Neuroprotectants for Epilepsy.
Review in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.
- Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management.International journal of molecular sciences · 2026Review
- Synchronized Imaging of Hydrogen Peroxide and Hydroxyl Radical in Pyroptosis and Epilepsy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Proanthocyanidins Alleviate T-2 Toxin-Induced Toxicity in Yak (Antioxidants (Basel, Switzerland) · 2026Article
- Curcumin nanoformulations in drug-resistant epilepsy: A mini review on mechanisms, preclinical evidence, and translational challenges.Molecular biology reports · 2026Review
- Mitochondria as a therapeutic target in neurodegeneration caused by hypoxia and ischemia during the perinatal period.Pharmacological reports : PR · 2026Review
- β-Amyrin Acetate Confers Anti-Epileptic Protection via Suppression of Calcium Overload-Induced Neuroinflammation and Apoptosis.Drug design, development and therapy · 2026Article
- Zingerone alleviates acute seizures by reducing intrinsic hippocampal neuronal excitability in a rat model of temporal lobe epilepsy.Frontiers in neuroscience · 2026Article
- Cardioprotective Effects of Soluble Guanylate Cyclase and Its α1 Subunit on Myocardial Ischemia/Reperfusion Injury via the PGC-1α/UCP2 Pathway.Journal of cardiovascular pharmacology · 2026Article
- Mitochondria as a Therapeutic Target in Neurodegeneration: Strategies for Restoring Cellular Homeostasis.Current neuropharmacology · 2026Review
- SAT1 Knockdown Decreases Glutamate-Induced Oxidative Stress, Ferroptosis, and Apoptosis in HT22 Cells via Activating the Nrf2/ARE Pathway.Neuromolecular medicine · 2025Article
- Transcriptomic decoding of regional cortical vulnerability to drug-resistant epilepsy using 7T MRI.Communications biology · 2025Article
- Dietary Antioxidant Quality Score and Epilepsy Odds in the US Adults: A Cross-Sectional NHANES Study.Brain and behavior · 2025Article
- Effects of nutrients and diet on mitochondrial dysfunction: An opportunity for therapeutic approaches in human disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Subacute Hypoxia Induces Cardiac Remodeling and Mitochondrial Dysfunction via Apoptotic Pathways in a Rabbit Model of Tracheal Stenosis.Journal of cardiovascular development and disease · 2025Article
- NLRP3 inflammasome: structure, mechanism, drug-induced organ toxicity, therapeutic strategies, and future perspectives.RSC medicinal chemistry · 2025Review
- Review
- Bursts of brain erosion: seizures and age-dependent neurological vulnerability.Trends in molecular medicine · 2025Review
- Mitochondrial dysfunction in epilepsy: mechanistic insights and clinical strategies.Molecular biology reports · 2025Review
- Neuroprotective Effects of Peanut Skin Extract Against Oxidative Injury in HT-22 Neuronal Cells.Pharmaceuticals (Basel, Switzerland) · 2025Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are major sources of reactive oxygen species (ROS) within the cell and are especially vulnerable to oxidative stress. Oxidative damage to mitochondria results in disrupted mitochondrial function and cell death signaling, finally triggering diverse pathologies such as epilepsy, a common neurological disease characterized with aberrant electrical brain activity. Antioxidants are considered as promising neuroprotective strategies for epileptic condition via combating the deleterious effects of excessive ROS production in mitochondria. In this review, we provide a brief discussion of the role of mitochondrial oxidative stress in the pathophysiology of epilepsy and evidences that support neuroprotective roles of antioxidants targeting mitochondrial oxidative stress including mitochondria-targeted antioxidants, polyphenols, vitamins, thiols, and nuclear factor E2-related factor 2 (Nrf2) activators in epilepsy. We point out these antioxidative compounds as effectively protective approaches for improving prognosis. In addition, we specially propose that these antioxidants exert neuroprotection against epileptic impairment possibly by modulating cell death interactions, notably autophagy-apoptosis, and autophagy-ferroptosis crosstalk.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.